Antihypertensive profile of cicletanine, a furopyridine derivative: comparison with captopril, indapamide and prazosin.

The effects of cicletanine were compared with those of three other antihypertensive drugs: prazosin, a highly selective alpha 1 antagonist, captopril an angiotensin converting enzyme inhibitor and indapamide a diuretic antihypertensive agent, on young stroke-prone SHR rats with high salt diet; furthermore, vascular reactivity to cicletanine was studied on isolated rat aorta. At an equal dose (30 mg/kg per os) all the drugs prevent the onset of hypertension with the same intensity. The minimal effective dose on blood pressure was 1 mg/kg for both cicletanine and captopril, and 3 mg/kg for indapamide.

Lack of effect of atrial natriuretic factor on the tone induced in rat portal vein by platelet-activating factor.

The spontaneous myogenic activity of the isolated rat portal vein was inhibited by atrial natriuretic factor or by sodium nitroprusside. These compounds were not effective on the tone induced by PAF-acether or carbachol. 8-Bromo cyclic GMP and dibutyryl cyclic AMP inhibited myogenic activity and reduced the agonist-induced contractions.

In vitro cardiovascular antihistamine properties of cicletanine in comparison with diphenhydramine.

Cicletanine (CIC) (pA2: 7.0) was found to be as potent as diphenhydramine (DIPH) (pA2: 7.2) in competitively inhibiting histamine-induced contraction of isolated rabbit aorta.

Endothelium-dependent vasorelaxation induced by Cn-acetal plasmalogens.

In this study the effects of the synthetic acetal plasmalogens (AP) C17-AP, C13-AP, C9-AP on isolated rabbit aorta were investigated with emphasis on their putative relationship with endothelium-dependent relaxing factor (EDRF). The various AP were obtained by total synthesis from the related fatty acid chlorides. In isolated rabbit aorta precontracted with phenylephrine (PE, 10(-7) M), C17-AP (greater than 10(-6) M) and C13-AP (greater than 10(-5) M) exerted an endothelium-dependent relaxation (EDR).

[Effects of Ginkgo biloba extract on 2 models of experimental myocardial ischemia].

Ginkgo biloba extract, a free radical scavenger containing kaempferol and quercetin esters, which are potent radical scavengers, was studied on various models of cardiac ischaemia, both in vitro and in vivo. On the two in vitro models of ischaemia-reperfusion described (rat and guinea-pig hearts) Ginkgo biloba extract was without effect on cardiac functional parameters. However, it induced a significant decrease in the intensity of ventricular fibrillation during the reperfusion stage.